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Drug-induced thyroid dysfunction
Published in David S. Cooper, Jennifer A. Sipos, Medical Management of Thyroid Disease, 2018
Victor Bernet, Robert C. Smallridge
Amiodarone is very rich in iodine: a 100 mg dose contains 37 mg of organic iodine and releases approximately 3.7 mg of free iodine into the circulation daily. It is associated with thyroid dysfunction in ~15–20% of individuals receiving this therapy (22). Thyroid disorders encountered with amiodarone therapy include amiodarone-induced hypothyroidism as well as thyrotoxicosis (amiodarone-induced thyrotoxicosis [AIT]) types 1 and 2. Type 1 AIT consists of iodine-induced hyperthyroidism while type 2 AIT represents a destructive thyroiditis, with the latter being the more common (23).
Investigation of Thyroid Disease
Published in John C Watkinson, Raymond W Clarke, Louise Jayne Clark, Adam J Donne, R James A England, Hisham M Mehanna, Gerald William McGarry, Sean Carrie, Basic Sciences Endocrine Surgery Rhinology, 2018
Thyroid ultrasound is now the most cost-effective approach to gaining structural information about the gland and is increasingly being performed by endocrinologists and surgeons, rather than being confined to use by radiologists.46, 47 Most benign thyroid diseases can be diagnosed by clinical presentation and appropriate blood tests, but colour-flow Doppler ultrasonography has utility in distinguishing between the hyperthyroid (type 1) and destructive (type 2) forms of amiodarone-induced thyrotoxicosis; blood flow is increased in the former and reduced in the latter.32
Answers
Published in John D Firth, Professor Ian Gilmore, MRCP Part 2 Self-Assessment, 2018
John D Firth, Professor Ian Gilmore
Amiodarone-induced thyroid dysfunction is a common problem in endocrine practice. As amiodarone interferes with deiodinase, free T4, free T3 and TSH should be considered together (high fT4 may be associated with low cellular fT3 levels). Amiodarone contains in excess of 35% iodine by weight and in patients with autoimmune subclinical hypothyroidism this may be sufficient to suppress thyroid function (the Wolff-Chaikov effect) leading to clinical hypothyroidism in about 6% of patients in iodine-replete populations. By contrast, in iodine deficiency Graves’ hyperthyroidism may be unmasked by sudden amiodarone (iodine) loading (type 1 amiodarone-induced thyrotoxicosis, the Jod-Basedow effect) and autonomy can develop in nodular goiters to drive thyrotoxicosis once iodine is replaced. Type 2 amiodarone-induced thyrotoxicosis is the result of inflammatory destruction of thyroid tissue and release of preformed hormone. This condition requires the initial use of high dose steroids to suppress it, and is most commonly associated with reduced or absent signal on scintigraphy. Thyroid ultrasonography with colour flow Doppler may be useful in distinguishing the absent vascular signal of type 2 from the normal or increased vascularity of type 1 thyrotoxicosis.
Takotsubo cardiomyopathy triggered by a single dose of flecainide in patient with focal atrial tachycardia
Published in Acta Cardiologica, 2022
Sonia J. Konsek-Komorowska, Piotr Cygański, Andrzej Rynkiewicz
The patient’s history revealed autoimmune thyroiditis in the euthyreosis phase for 10 years, and two recent electrophysiological studies in which focal AT could not be triggered or observed. The patient had contracted an upper respiratory tract infection 4 months prior to admission, and subsequently experienced a couple of episodes of focal AT in the intervening period, lasting for more than one day, and not treatable by vagal manoeuvres. Intravenous pharmacological intervention was required to terminate the arrhythmia using adenosine, metoprolol, propafenone, verapamil, amiodarone, antazoline administered alone or in different combination. Repeated transthoracic echocardiography (TTE) measurements were within normal limits, left ventricular global systolic function was normal, and no regional wall motion abnormalities were seen at the time. Based on the patient’s clinical features, a history of occasional amiodarone intake, increased level of total serum thyroxine (T4), amiodarone-induced thyrotoxicosis (AIT) was suspected.
Updates in the management of congenital heart disease in adult patients
Published in Expert Review of Cardiovascular Therapy, 2022
Danielle Massarella, Rafael Alonso-Gonzalez
Antiarrhythmic drugs are less efficient in patients with congenital heart disease than in patients with acquired heart disease. In addition, these patients are at higher risk of developing toxicity, i.e. amiodarone-induced thyrotoxicosis occurs in 47% of Fontan patients [14]. As such, it is reasonable to consider catheter ablation early after onset of a sustained atrial arrhythmia. Despite the demonstrable success of this approach, there are several challenges unique to this patient population [15]. As a result of previous surgical repair or previous multiple interventions, both vascular access and access to the intracardiac structures can be limited. Moreover, catheter manipulation can be difficult due to anatomic complexity or extensive atrial enlargement. Finally, due to the high prevalence of multiple arrhythmia, procedure time tends to be increased [15]. Consequently, success rates for complex ablations (such as in congenital heart disease) are reduced, and risk of short-term recurrence is increased [15–17]. The application of novel modalities to augment the success of ablation in patients with complex anatomy, such as 3D mapping, robotic magnetic navigation and noninvasive stereotactic arrhythmia radioablation, hold promise for application in the congenital heart disease population [15,18–21]. Although outcome data are limited for some of these techniques, several publications have suggested that magnetic navigation is safe and feasible in the setting of complex congenital heart disease and increases the rate of success in this complex population [15,22–24].
Usefulness of plasmapheresis in patients with severe complicated thyrotoxicosis
Published in Baylor University Medical Center Proceedings, 2021
Myrian Vinan-Vega, Barbara Mantilla, Nusrat Jahan, Cabandugama Peminda, Kenneth Nugent, Joaquin Lado-Abeal, Ana Rivas
Patients who do not respond to standard therapy and in whom the effects of severe thyrotoxicosis persist despite medical management may warrant emergent thyroidectomy,2,3,7,10 for which an euthyroid state is preferable prior to surgical intervention to achieve better results.11 Alternative measures should be used as a bridge for urgent thyroidectomy. Plasmapheresis involves the extracorporeal separation of plasma from the blood. By using the centrifugation technique, plasma is separated from the cellular components of the blood and discarded. Later, cellular components are returned to the patient along with replacement fluid, such as plasma, albumin, and crystalloid.12,13 Plasmapheresis is a quick and efficient way to remove pathological proteins, including autoantibodies, paraproteins, and cytokines, from the circulation.14 According to the American Society for Apheresis, it can be considered a therapeutic option in the setting of complicated thyrotoxicosis in patients with severe symptoms and rapid clinical deterioration, failure of conventional therapies, contraindications to other therapies, or multiorgan decompensation.4,15,16 Additionally, given amiodarone’s long half-life, plasmapheresis is used to lower amiodarone plasma concentrations in patients with amiodarone-induced thyrotoxicosis, particularly in those with no underlying thyroid pathology who develop drug-induced destructive thyroiditis.10,14,17,18